Chromosomal instability and aging : basic science and by Fuki Hisama, Sherman M. Weissman, George M. Martin

By Fuki Hisama, Sherman M. Weissman, George M. Martin

This article examines the connection among DNA harm and service, mobile senescence, genomic instability, and getting older. The authors offer in-depth discussions of assorted sorts of DNA harm, the DNA fix community, and mobile responses to genetic harm to evaluate their effect at the modulation of getting older tactics and age-related ailments, together with melanoma improvement. Chromosomal Instability and getting older describes cloning genes for human chromosomal instability problems, the causal elements and results of chromosomal damage, the telomere speculation of getting older, and age-dependant mitochondrial genetic instability. It comprises greater than 2200 references to facilitate additional study, making it an informative and well timed advisor.

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One example is cells from humans with the Li-Fraumeni syndrome, a hereditary cancer-prone syndrome caused by mutations in p53 (159,160). These cells immortalize at a frequency that is well above the vanishingly low immortalization frequency of normal fibroblasts (161). Thus, there is increasing evidence that cellular senescence constitutes an important defense against the development of cancer in mammals, including humans. Hanahan and Weinberg have proposed that cells must acquire a defined number of traits for a malignant tumor to form: unregulated growth (hypersensitivity to positive signals, resistance to inhibitory signals), resistance to apoptosis, unlimited replicative potential, angiogenesis, invasion, and metastasis (9).

Many telomerase-positive tumor cells also proliferate indefinitely with very short telomeres. These findings suggest that telomerase may act preferentially on the shortest telomeres. The mechanisms by which dysfunctional telomeres signal cells to undergo cellular senescence or cell death are poorly understood. B. DNA Damage Certain types and/or levels of damage to genomic DNA can cause normal mammalian cells to undergo a senescence arrest. This damage may derive from endogenous or exogenous sources and includes DNA base and sugar modifications as well as single- or double-strand breaks in the DNA (19,20,24).

These findings suggest that telomerase may act preferentially on the shortest telomeres. The mechanisms by which dysfunctional telomeres signal cells to undergo cellular senescence or cell death are poorly understood. B. DNA Damage Certain types and/or levels of damage to genomic DNA can cause normal mammalian cells to undergo a senescence arrest. This damage may derive from endogenous or exogenous sources and includes DNA base and sugar modifications as well as single- or double-strand breaks in the DNA (19,20,24).

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